Ionic basis of the different action potential configurations of single guinea‐pig atrial and ventricular myocytes.

Abstract

SUMMARY1. Single myocardial cells were enzymatically dispersed from guinea-pig atria and ventricles. At 25 0C, atrial cell action potentials differed significantly from ventricular cell action potentials in duration (atrial = 141 ms, ventricular = 497 ms) and overshoot (atrial = + 36 mV, ventricular = +42 mV).2. (Hume & Giles, 1983), or larger tip diameter pipettes, with internal dialysis (Hamill, Marty, Neher, Sakmann & Sigworth, 1981).4. Two significant differences in background K+ conductance in single atrial and ventricular myocytes were observed: (i) the isochronal (5 s 8. The rate of decay of ica was examined in ventricular myocytes, in which both time-dependent outward current and inward-rectifying K+ current were blocked by intracellular loading of caesium. iCa decay was non-exponential and lasted as long as 400 ms at + 20 mV. The decay could be described as the sum of two exponentials, the time constants of which were both U-shaped functions of membrane potential.9. It is concluded that different properties of resting K+ channels contribute significantly to the different action potential configurations of single atrial and ventricular myocytes. The time course of the plateau of the ventricular action potential is importantly determined by both the rate of decay of ica at positive membrane potentials and activation of time-dependent outward current. In atrial cells, the amplitude of iCa may be shunted due to the absence of a negative slope conductance region in the background current-voltage relationship.

Quantification of exponential Na+ current activation in N‐bromoacetamide‐treated cardiac myocytes of guinea‐pig.

“…The Vmax was 280 6 + 24 1 V s-1 (n = 6) at around 0 mV, which was similar to the value in rat ventricular cells (230 V s-1: Brown, Lee & Powell, 1981). Smaller values as previously reported in the guinea-pig ventricular cells (808 + 177 V s-1 at 25 C, Hume & Uehara, 1985) were observed only when the resting potential was less negative than -80 mV, and were not used in the present study. The Vmax was not different whether the action potential was initiated immediately or 4 ms after the end of the current injection (not shown), which suggested a very slow development of inactivation at potentials negative to that of the Na+ current activation.…”

The temperature dependence of electrical excitability in fish hearts

“…Although such comparisons are problematic, because APD is strongly dependent on body mass and f H in mammals, and physiological body temperatures of fishes and mammals seldom overlap, some supportive evidence can be provided. For example, the APD of the brown trout ventricular myocytes is 85 ms at +25°C and only 26 ms at +35°C , whereas in the similar-sized guinea pig, the APD of ventricular myocytes is 496 and 250 ms at +35°C and +25°C, respectively (Hume and Uehara, 1985), despite the higher f H in guinea pig (resting f H of 230-300 beats min −1 ) than brown trout (maximal f H =124 beats min −1 ) (Rouslin et al, 1995;Vornanen et al, 2014). Similarly, the ventricular APD 50 of the zebrafish, a species tolerating temperatures as high as +40°C (Cortemeglia and Beitinger, 2005), is only ∼60 ms at +36°C, which is much shorter than the ventricular AP of most laboratory mammals (200-300 ms at +34°C) with comparable f H values (Rosati et al, 2008;Vornanen and Hassinen, 2016).…”

Significance of Na+ current in the excitability of atrial and ventricular myocardium of the fish heart

“…The atrial muscle excitation wave enters the ventricular myocardium, where it produces even quicker rising and more prolonged APs. This sequence of events requires a particular composition of membrane currents from each myocyte type to enable adequate excitability for each cardiac compartment and tuning of excitability and impulse conduction to the unique contractile properties of atrial and ventricular myocardium (Hume and Uehara, 1985;Schram et al, 2002;Marionneau et al, 2005).…”